Heart failure refers to the heart's inability to keep up with the demands made upon it. Congestive heart failure refers to an inability of the heart to pump an adequate amount of blood to the body tissues. Because the heart is unable to pump an adequate amount of blood, blood returning to the heart becomes congested in the venous and pulmonary system.
In a healthy heart, the heart pumps all of the blood that returns to it, according to the Frank-Starling law. Increased venous return leads to increased end diastolic volume, which causes increased strength of contraction and increased stroke volume. In addition to intrinsic control according to the Frank-Starling law, a healthy heart is subject to extrinsic control, such as stimulation by the sympathetic nervous system to enhance contractility.
In a patient experiencing congestive heart failure, intrinsic and extrinsic control mechanisms may not function properly, and consequently the heart may fail to pump an adequate amount of blood. A condition known as cardiac decompensation is used to describe heart failure that results in a failure of adequate circulation.
Failure of the left side of the heart is generally more serious than the failure of the right side. On the left side of the heart, blood returns from the pulmonary system and is pumped to the rest of the body. When the left side of the heart fails, there are consequences to both the pulmonary system and to the rest of the body. A patient with congestive heart failure may be unable to pump enough blood forward to provide an adequate flow of blood to his kidneys, for example, causing him to retain excess water and salt. His heart may also be unable to handle the blood returning from his pulmonary system, resulting in a damming of the blood in the lungs and increasing his risk of developing pulmonary edema.
Causing more blood to be expelled from the heart, i.e., increasing cardiac output would increase the blood flow to the organs and tissues and reduce the risk of damming of blood in the lungs caused by heart failure. Patients with congestive heart failure are often treated with drug therapy intended to increase their cardiac output. Drugs administered to treat congestive heart failure by increasing cardiac output often have a positive inotropic effect on the heart. Drugs that have a positive inotropic effect on the heart increase cardiac output by increasing the contractility of the heart, which causes the heart to beat more forcefully, which in turn causes the ventricles of the heart to eject more blood per stroke. Drugs that have a positive inotropic effect on the heart include cardiac glycosides such as digitalis, digoxin and digitoxin, beta-adrenergic agonists such as dopamine and dobutamine, and phosphodiesterase inhibitors such as amrinone and milrinone.
Often, a physician determines a course of drug therapy for a patient with congestive heart failure based on the patient's condition during an admission or office visit. The drugs to be administered and the dosages for those drugs are chosen at that time. The drugs may then be self-administered or administered via an implanted drug delivery device. In some cases, congestive heart failure patients frequently visit the physician's office to have their condition evaluated. At these visits, the patient may receive a supplemental drug or dosage or otherwise have the drug therapy modified as indicated by his condition. This situation may be very costly because of the hospital stay, nursing costs, patient transportation costs, and so forth.
Further, frequent visits fail to recognize changes in the patient's condition between visits. These changes may indicate an increased or decreased need for drug therapy that increases cardiac output. Because these changes are not recognized, the drug therapy is not modified to address them. If the changes indicate a worsening of the patient's condition and a need for increased cardiac output, failure to address them promptly may endanger the patient.
Therefore, there is a need for a system and method to monitor a congestive heart failure patient's condition, and appropriately modify the patient's drug therapy as a function of the patient's condition, in an outpatient setting.
Some existing methods monitor a patient's condition with an implanted physiological sensor, and control the operation of an implanted drug delivery device as a function of the patient's condition as measured by the physiological sensor. For example, U.S. Pat. No. 4,003,379, issue to Ellinwood, Jr., discloses controlling an implanted drug delivery device to deliver hypertension medication in response to blood pressure as measured by a pressure transducer implanted in the neck or lower extremities.
Some existing methods for monitoring a patient's condition in an outpatient situation use an implanted pressure monitor and sensor to estimate the patient's pulmonary artery diastolic pressure as a function of the blood pressure in the patient's right ventricle. For example, U.S. Pat. No. 5,368,040, issued to Carney, discloses a system that includes an implanted pressure monitor that can estimate the pulmonary artery diastolic pressure from a pressure signal received from a pressure sensor in the right ventricle. Further, U.S. Pat. No. 6,155,267, to Nelson, discloses using the occurrence of a change in the state of a physiological parameter, such as estimated pulmonary artery diastolic pressure, as a trigger to change the dosage of a drug delivered by an implanted drug delivery device.
None of the existing methods, however, disclose a system and method to monitor a congestive heart failure patient's condition and appropriately modify the patient's drug therapy as a function of the patient's condition in an outpatient situation. None of the existing methods disclose how to relate a measured intra-cardiac pressure, such as the estimated pulmonary artery diastolic pressure, to the congestive heart failure patient's need for increased cardiac output. Further, none of these methods disclose how to modify the drug therapy as a function of the measured pressure to meet this need.
Examples of the above referenced existing techniques and/or devices may be found in the issued U.S. Patents listed in Table 1 below.
TABLE 1U.S Pat. No.InventorIssue Date6,155,267NelsonDec. 05, 20006,024,704Meador et al.Feb. 15, 20005,810,735Halperin et al.Sep. 22, 19985,626,623Kievel et al.May 06, 19975,564,434Halperin et al.Oct. 15, 19965,535,752Halperin et al.Jul. 16, 19965,368,040CarneyNov. 29, 19945,135,178MarokoOct. 06, 19924,003,379Ellinwood, Jr.Jan. 18, 1977
All patents listed in Table 1 above are hereby incorporated by reference herein in their respective entireties. As those of ordinary skill in the art will appreciate readily upon reading the Summary of the Invention, Detailed Description of the Preferred Embodiments and claims set forth below, many of the devices and methods disclosed in the patents of Table 1 may be modified advantageously by using the techniques of the present invention.